Free Access
Vet. Res.
Volume 31, Number 1, January-February 2000
Page(s) 57 - 58
How to cite this article Vet. Res. (2000) 57-58
Vet. Res. 31 (2000) 57-58

The pathogenesis of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) in the boar

J. Christopher-Hennings

South Dakota State University, Animal Disease Research and Diagnostic laboratory, Box 2175, N. Campus Drive, Brookings, SD 57007, USA

Abstract - Boars are important in the transmission of PRRSV through boar semen and this has been demonstrated in both experimental and field studies. Due to the importance of preventing PRRSV transmission through boar semen, the objectives in our studies have focused on the development of molecular techniques to detect PRRSV in semen. We then used these techniques in determining the relationships between viremia, serologic status and shedding of PRRSV in semen; identifying persistent shedding of PRRSV in boar semen; evaluating the effects of a modified-live PRRSV vaccine in boars; and determining the origin of PRRSV in semen. For these studies, 22 boars have been utilised as either PRRSV inoculated or control boars. A nested reverse-transcriptase polymerase chain reaction (RT- PCR) was developed for use on semen, serum and porcine tissues for the detection of PRRSV. This assay correlated well with a "swine bioassay" which detects the presence of infectious virus in boar semen. By using RT-PCR on semen and serum we determined that the PRRSV serostatus of the boar does not always correlate with viremia or shedding of PRRSV in semen. Persistence of PRRSV shedding in semen has also been demonstrated for as long as 92 days post inoculation with wild-type virus. The modified-live PRRSV vaccine can be shed in semen for as long as 39 days post vaccination, however, 3 of 5 vaccinated boars only shed vaccine virus 1-3 times within the first 2 weeks after vaccination. At 50 days post vaccination, when these boars were challenged with a wild-type PRRSV isolate, the vaccine either eliminated PRRSV shedding in semen or reduced the duration of shedding in 4 of 5 boars. However, semen quality was compromised in the vaccinated boars, compared to non-vaccinates. Using vasectomized boars, fractionation of semen, and immunohistochemistry, the suggested mechanism for PRRSV entry into boar semen may primarily be through systemic distribution to monocytes and tissue macrophages into semen and not exclusively through replication in the testis and epididymis. Since PRRSV in semen has been demonstrated to be infectious and serostatus and viremia are not reliable indicators of PRRSV shedding in semen, testing boar semen for PRRSV or retaining PRRSV naïve boars in strict biosecurity appear to be the primary methods of PRRSV control in boar studs. Vaccination of boars with a modified-live PRRSV vaccine may reduce or eliminate wild-type PRRSV shedding in semen, but the vaccine itself may still be shed and the duration of immunity and sperm quality effects may require further study to warrant the vaccination of boars. Finally, since vasectomized boars can shed PRRSV in semen, there appears to be a systemic mechanism of viral entry into semen. Macrophages are the primary cell type infected with PRRSV within the semen. Further studies of factors which influence the infection of these cells, their entry into semen and host mechanisms of resistance and viral clearance in the boar will be important in preventing the transmission of PRRSV in boar semen.

Corresponding author: J. Christopher-Hennings Tel: (1) 605 688 4317; fax: (1) 605 688 6003;

© INRA, EDP Sciences 2000